椎管内硬脊膜外囊肿1例

病历摘要患者，男，22岁。1月前无明显诱因出现双下肢无力．以右侧为重。4d后症状加重。神经系统查体：左下肢肌力Ⅲ级，右下肢Ⅱ级，肌张力增高。双侧膝反射（），病理症阳性。胸椎X光片示胸8~9椎弓根受压变形，间距加大。椎体后缘骨质结构欠完整，可见弧形压迹。MRI示胸4~9区     

人脑胶质瘤nm23-H1蛋白及PCNA的表达

目的　研究人脑胶质瘤中nm2 3 H1蛋白和增殖细胞核抗原 (PCNA)表达状况。方法　采用免疫组化染色技术 ,对 5 3例人脑胶质瘤石蜡切片中nm2 3 H1蛋白和PCNA进行检测。结果　 5 3例人脑胶质瘤免疫组化染色结果显示 ,人脑胶质瘤I级、II级中nm2 3 H1阳性细胞显著高于Ⅲ、Ⅳ级 (P <0 .0 5 ) ;Ⅲ、Ⅳ级中PCNA阳性细胞显著高于I、II级(P <0 .0 5 ) ,但PCNA蛋白表达与nm2 3 H1表达无显著相关性。结论　nm2 3 H1蛋白低表达及PCNA高表达与脑胶质瘤的病理学分级相关 ;nm2 3 H1表达可能成为脑胶质瘤的浸润与转移的指标。     

THE EXPERIMENTAL STUDY ON THE CELL APOPTOSIS AND EXPRESSION OF BCL-2 PROTEIN IN INTRACEREBRAL HEMORRHAGE IN MODEL OF RATS

Intra-cerebral hemorrhage is a common clinicaldisease,with a high mortality and morbidity.So itis one of the clinical hot topics.It has been foundinrecent years that there is a close relationship bet weenthe cell apoptosis and the course or prognosis of in-tra-cerebral hemorrhage.Bcl-2,as the apoptosis-adjusted gene,plays ani mportant role in the courseof cell apoptosis,but the mechanis min the cell ap-optosis in intra-cerebral hemorrhage remains un-clear.In this experi ment,with the model bui…     

椎管内硬脊膜外恶性血管外皮瘤1例报告

<正> 患者,男性,35岁。1989年2月3日因进行性双下肢麻木,活动不灵20多天,加重伴小便困难,1周余入院。检查:第9胸髓平面以下痛、温觉减退,双下肢肌力均弱,右下肢Ⅲ级,左下肢Ⅱ级.腱反射对称亢进,双侧巴氏征阳性。腰穿脑脊液无色清亮,蛋白2.78g/L,细胞数正常,椎管腔呈完全性梗阻。脊柱平片显示     

Induction of apoptosis and inhibition of proliferation of C6 glioma cells in vitro by tamoxifen

Objective To investigate the anti-tumor effect and mechanism of tamoxifen on rat C6 glioma cells. Methods C6 cells were cultured in Dulbecco＇s modified Eagle＇s medium （DMEM） with 3% fetal calf serum （FCS）, and treated with tamoxifen of different concentrations, i.e. group A （1.25 μmol/L）, group B （2.50 μmol/L）, group C （5. 00 μmol/L）, group D （10. 00 μmol/L）, group E （20. 00 μmol/L） and control group （0. 00 μmol/L）. Morphological changes, MTT assay and 5-bromo-2＇-deoxyuriding labeling ratio were assessed. Apoptosis was observed by flow cytometry. Results C6 cells treated with different doses of tamoxifen for 24, 48, and 72 hours became irregular in shape, while cells treated with vehicle grew normally. MTT assay showed that tamoxifen did not suppress C6 cell growth until 72 hours after treatment. Seventy-two hours after treatment, there were significant differences in cell viable rate between group A versus groups C, D and E; so did group B versus group D as well as group E （P〈 0.05 ）. BrdU incorporation assay indicated significant difference of BrdU labbled index （BrdU LI） among groups A, C, E and control group 48 hoers after treatment （P〈0.05）. And the BrdU LI decreased with the increased concentration of tamoxifen. Flow cytometry （FCM） showed significant difference between treated group and control group at 24, 48, and 72 hours after treatment （P〈0.05）. Conclusion Tamoxifen significantly suppresses the growth of C6 glioma cells in a time- and dose-dependent manner. The mechanism of tamoxifen suppressing C6 glioma cells may be inhibiting proliferation and inducing apoptosis. Therefore, tamoxifen can be a candidate as a chemotherapy agent for glioma.